Keratinocyte prostaglandin synthesis is enhanced by IL-1.
Keratinocytes are a rich source of IL-1, a cytokine which stimulates prostaglandin synthesis in many cell types. The effects on arachidonic acid metabolism of this cytokine were therefore studied in cultured adult human keratinocytes. Exogenous IL-1 increased basal cellular prostaglandin synthesis (particularly PGE2) threefold. Increased PGE2 synthesis in response to IL-1 was inhibited by cycloheximide, suggesting a requirement for new protein synthesis. Irradiation of the keratinocytes with low-dose ultraviolet light B (UVB) resulted in the release of increased quantities of both IL-1 and PGE2. The amount of IL-1 released was sufficient to increase PGE2 synthesis when exogenously added to unstimulated cells, suggesting a causal relationship. The time course of accumulation of IL-1 and PGE2 in the medium of irradiated keratinocytes was also consistent with a cause-effect relationship. No feedback inhibition of IL-1 release by the increased PGE2 was detected as demonstrated by the observation that IL-1 production in response to UVB was not augmented by treatment with indomethacin or blunted by the exogenous addition of PGE2. These data suggest that keratinocyte IL-1 may be partially responsible for induction of keratinocyte PGE2 synthesis after UVB irradiation.
Pentland
A P
AP
Division of Dermatology, Washington University School of Medicine, St. Louis, Missouri 63110.
Mahoney
M G
MG
D002855:Chromatography, Thin Layer; D015232:Dinoprostone / Q000096:biosynthesis / Q000502:physiology; D004347:Drug Interactions; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism / Q000494:pharmacology*; D015603:Keratinocytes / Q000378:metabolism*; D011453:Prostaglandins / Q000096:biosynthesis*; D013997:Time Factors
D007375:Interleukin-1; D011453:Prostaglandins; D015232:Dinoprostone